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PubMed1997

Cellular mechanisms mediating rat renal microvascular constriction by angiotensin II.

To assess cellular mechanisms mediating afferent (AA) and efferent arteriolar (EA) constriction by angiotensin II (AngII), experiments were performed using isolated perfused hydronephrotic kidneys. In the first series of studies, AngII (0.3 nM) constricted AAs and EAs by 29+/-3 (n = 8, P < 0.01) and 27+/-3% (n = 8, P < 0.01), respectively. Subsequent addition of nifedipine restored AA but not EA diameter. Manganese (8 mM) reversed EA constriction by 65+/-9% (P < 0.01). In the second group, the addition of N-ethylmaleimide (10 microM), a Gi/Go protein antagonist, abolished AngII- induced EA (n = 6) but not AA constriction (n = 6). In the third series of experiments, treatment with 2-nitro-4-carboxyphenyl-N, N-diphenyl-carbamate (200 microM), a phospholipase C inhibitor, blocked both AA and EA constriction by AngII (n = 6 for each). In the fourth group, thapsigargin (1 microM) prevented AngII-induced AA constriction (n = 8) and attenuated EA constriction (8+/-2% decrease in EA diameter at 0.3 nM AngII, n = 8, P < 0.05). Subsequent addition of manganese (8 mM) reversed EA constriction. Our data provide evidence that in AAs, AngII stimulates phospholipase C with subsequent calcium mobilization that is required to activate voltage-dependent calcium channels. Our results suggest that AngII constricts EAs by activating phospholipase C via the Gi protein family, thereby eliciting both calcium mobilization and calcium entry.

Angiotensin II↗
PubMed1989

Influence of carotid chemoreceptors on the vagal reflex-induced tracheal constriction.

In this study, the effects of carotid chemoreceptors on reflex tracheal constriction were investigated in anesthetized, paralyzed, and artificially ventilated mongrel dogs. Reflex tracheal constriction was measured as changes in the intratracheal pressure of an air-filled balloon introduced into the rostral side of the transected trachea. A hypoxic condition was produced by ventilating the dog with 12% O2-88% N2. The reflex tracheal constriction induced by histamine inhalation to the bronchial side was reduced by section of the bilateral sinus nerves. The hypoxic condition significantly potentiated the reflex tracheal constriction induced by histamine inhalation. The potentiated reflex tracheal constriction during hypoxia was abolished by section of the bilateral sinus nerves. The afferent electrical stimulation to the central cut end of the vagus nerve caused a reflex tracheal constriction. The reflex tracheal constriction was significantly potentiated by hypoxia, and the potentiating response was abolished by section of the bilateral sinus nerves. The infusion of NaCN into the bilateral carotid arteries significantly potentiated the reflex tracheal constriction. The NaCN-induced potentiating effect was abolished by section of the bilateral sinus nerves. These results suggest that hypoxia potentiates the vagal reflex-induced tracheal constriction and that the hypoxia-induced potentiating effects may be mediated by carotid chemoreceptors.

Administration, Inhalation↗
PubMed2003

Effects of bronchial intermittent constrictions on explosive flow during coughing in the dogs.

This study tested the hypothesis that intrathoracic bronchi intermittently constrict during coughing and attempted to elucidate the effect on explosive flow. The subjects were 21 dogs having undergone tracheostomy. In the first group A (n = 7), the diameter of the fifth-generation bronchus was measured with a balloon-tipped catheter and the change during coughing was analyzed. In the other group (n = 14), the dogs were vagotomized and coughing was simulated by sequential application of positive and negative airway pressures (sham cough). The effects of the bronchial constriction, elicited by the stimulation of vagus efferent fibers, on explosive flow and airway pressure of sham cough were analyzed. The bronchus was constricted in explosive phase of spontaneous coughing in all the dogs of the first group. When cough bouts were repetitively developed, bronchial constriction and phrenic burst developed simultaneously. The intermittent bronchial constrictions fused and virtually acted as tonic constriction. In the second group of dogs the explosive flow of sham cough consisted of two phases; a short bout followed by a near-constant flow. When the bronchus was constricted, the explosive flow was still biphasic in 12 dogs and an exponential decay pattern formed in 2 of them. In these 12 dogs, the peak explosive flow slightly but significantly decreased (mean +/- SD, 1.39 +/- 0.23 vs. 1.34 +/- 0.23 l/s) and airway pressure in the segmental bronchus became smaller (-1.18 +/- 0.53 vs. -0.15 +/- 0.94 cmH(2)O). We concluded that intermittent bronchial constrictions act as tonic one during coughing. Bronchial constriction slightly decreased the peak explosive flow and moved the choke point to the proximal airway.

Animals↗
PubMed1995

Constrictive pericarditis: its history and current status.

The diagnosis of constrictive pericarditis remains a challenge because it is often mimicked by restrictive cardiomyopathy. The last few years have seen numerous advances in our ability to differentiate between these two conditions which often have similar physical findings and hemodynamics. This review begins with a brief history of constrictive pericarditis; this is followed by an extensive discussion of newer etiologies, and then the classical clinical history and physical examination findings are described. Radiologic, electrocardiographic, and angiographic findings are discussed. The hemodynamics of constrictive pericarditis are reviewed. Recent results of echocardiographic and echo-Doppler investigations are presented. Emphasis is placed upon the limitations of M-mode echocardiography in the diagnosis of constrictive pericarditis. The value of echocardiographic Doppler studies of mitral and tricuspid flow velocity patterns, as well as of those in the pulmonary veins and hepatic veins, is described. Nuclear ventriculograms and angiocardiograms tend to show more rapid ventricular filling in constrictive pericarditis than in restrictive cardiomyopathy. Although only a small number of patients has been studied, these evaluations seem to have merit in separating restrictive cardiomyopathy from constrictive pericarditis. The role of computed tomography scanning and magnetic resonance imaging studies of pericardial thickness in confirming the presence of constrictive pericarditis is discussed. Abnormal pericardial thickening (> 3 mm) confirms the diagnosis of constrictive pericarditis, but only if the characteristic hemodynamic pattern is present. The usefulness of endomyocardial biopsy in recognizing specific varieties of restrictive cardiomyopathy is presented.(ABSTRACT TRUNCATED AT 250 WORDS)

Diagnosis, Differential↗
PubMed1994

Diagnostic role of Doppler echocardiography in constrictive pericarditis.

OBJECTIVES: This study was conducted to assess the diagnostic role of Doppler echocardiography in constrictive pericarditis. BACKGROUND: It has been observed that patients with constrictive pericarditis have a characteristic Doppler pattern of respiratory variation in ventricular filling and central venous flow velocities. However, the observation was based on a small number of patients with known diagnosis. METHODS: We reviewed the echocardiographic features of 28 patients (21 men and 7 women; mean age +/- SD 55 +/- 15 years) with suspected constrictive pericarditis who underwent exploratory thoracotomy or pericardiectomy. RESULTS: At operation, constrictive pericarditis was diagnosed in 25 patients, restriction in 1 and normal pericardium in 2. Of the 25 patients with constriction, correct preoperative Doppler diagnosis was made in 22 (88%) and Doppler echocardiography showed restriction in 3. In two patients with a normal pericardium, Doppler features were consistent with constriction in one patient and were normal in the other. In the one patient with restriction, Doppler echocardiography showed restriction. In 19 patients with surgically proved constriction, repeat Doppler study after pericardiectomy showed normal findings in 14 and restriction in 5. Twelve of the 14 patients with normalized Doppler findings became asymptomatic, whereas all 5 with restrictive Doppler features remained symptomatic. CONCLUSIONS: Doppler echocardiography performed simultaneously with respiratory recording is highly sensitive for diagnosing constrictive pericarditis, and it appears to predict functional response to pericardiectomy.

Adult↗
PubMed2004

The effect of umbilical venous constriction on placental development, cord length and perinatal outcome.

BACKGROUND: Umbilical vein constriction at the fetal abdominal inlet is a common finding after week 13, when the period of umbilical herniation is brought to an end. AIMS: To test the hypothesis that a constricting umbilical ring within physiological ranges affects fetal hemodynamics by either pooling blood in the placenta or restricting nutrient transfer to the fetus and thus shift the birthweight/placental weight (BW/PW) ratio. A constriction could also cause pressure changes and elongation of the cord and possibly be a disadvantage during labour. STUDY DESIGN: Cross-sectional. SUBJECTS: 359 Low-risk singleton pregnancies at 13-40 weeks of gestation. OUTCOME MEASURES: Standard deviation score (z-score) and regression analysis were used to determine the effect of umbilical vein constriction (expressed by increased blood velocity) on birthweight/placental weight ratio (BW/PW), cord length, Apgar score and emergency delivery due to fetal distress. RESULTS: Umbilical venous constriction had a mild but significant effect on BW/PW in male (p=0.018) but not in female fetuses. Increased constriction was also associated with increased length of the cord but only in female fetuses (p=0.019). Cord length was positively related to birthweight and placental weight, but an increased length of the cord was also associated with decreasing BW/PW ratio for the male fetuses only (p=0.044). Increasing degree of venous constriction was associated with Apgar score < or =7 at 1 (p=0.009) but not at 5 min after birth and was not associated with emergency delivery. CONCLUSION: Physiological umbilical venous constriction exerts a mild but significant gender-specific hemodynamic impact on intrauterine development.

Adolescent↗
PubMed1997

Doppler echocardiographic evaluation of ventricular diastolic filling in fetuses with ductal constriction.

To assess ventricular diastolic filling in fetuses with constriction of ducts arterious, 43 fetuses of pregnant women receiving indomethacin (100 to 150 mg/day) were examined with Doppler echocardiography. Ductal constriction occurred in 21 fetuses, defined as maximal systolic velocity > 140 cm/s and diastolic flow velocity > 30 cm/s. The variables measured to assess diastolic function were peak velocity during early diastole (peak E wave), peak velocity during atrial contraction (peak A wave), and the velocity ratio (peak E/A ratio); these were compared to maximal ductal flow velocity during systole and diastole. The mitral peak E wave, peak A wave, and peak E/A ratio in fetuses with ductal constriction showed no significant difference from those in fetuses without ductal constriction. In fetuses with ductal constriction, the tricuspid A wave increased significantly without changes in the peak E wave (57 +/- 9 vs 50 +/- 6 cm/s, p < 0.01) and the peak E/A ratio was significantly lower than in fetuses without ductal constriction (0.57 +/- 0.10 vs 0.65 +/- 0.08, p < 0.05). In 9 fetuses with ductal constriction, we compared the Doppler tricuspid E wave, A wave, and E/A ratio during indomethacin administration with those after withdrawal of the drug for a mean of 24 hours. Both systolic and diastolic ductal flow velocities in the fetuses returned to normal range after discontinuation of indomethacin. The tricuspid peak A wave decreased (59 +/- 9 vs 50 +/- 11 cm/s) and the E/ A ratio increased significantly (0.56 +/- 0.07 vs 0.69 +/- 0.07) (both p < 0.01) without any significant change in peak E wave after discontinuation of indomethacin. This study suggests that ductal constriction influences Doppler patterns of right ventricular diastolic filling. These changes could be related to the increased afterload presented to the right ventricle which might affect diastolic function.

Anti-Inflammatory Agents, Non-Steroidal↗
PubMed1998

Comparison of mitral inflow and superior vena cava Doppler velocities in chronic obstructive pulmonary disease and constrictive pericarditis.

OBJECTIVE: This study was conducted to determine whether Doppler recording of superior vena cava flow velocities can differentiate chronic obstructive pulmonary disease from constrictive pericarditis in patients with a respiratory variation of > or = 25% in mitral inflow E velocity. BACKGROUND: Although respiratory variation (> or = 25%) in mitral E velocity is the main diagnostic criterion for constrictive pericarditis by Doppler echocardiography, it can also be present in chronic obstructive pulmonary disease. Because the respiratory variation is due to increased change in intrathoracic pressure with respiration in chronic obstructive pulmonary disease, and to dissociation of intrathoracic-intracardiac pressure changes in constriction, it was hypothesized that the Doppler flow velocity pattern in the superior vena cava (affected by intrathoracic pressure) would be different in these two conditions. METHODS: Pulsed-wave Doppler recording of mitral and superior vena cava flow velocities in 20 patients with chronic obstructive pulmonary disease who had > or = 25% respiratory variation in mitral E-wave velocity were compared with those of 20 patients who had surgically proved constrictive pericarditis. RESULTS: Constrictive pericarditis and chronic obstructive pulmonary disease had similar respiratory variation in mitral E velocity (41% versus 46%). In the latter, the E/A ratio was lower (inspiration, 0.8+/-0.3 versus 1.5+/-0.7 [p < 0.0001]; expiration, 1.0+/-0.3 vs. 1.9+/-0.7 [p < 0.0001]) and deceleration time longer (inspiration, 198+/-53 ms versus 137+/-32 ms; expiration, 225+/-43 ms vs. 161+/-33 ms [p < 0.0001]). Inspiratory superior vena cava systolic forward flow velocity was significantly higher in chronic obstructive pulmonary disease (72.9+/-22.6 cm/s versus 36.2+/-9.3 cm/s, p < 0.0001), while expiratory systolic forward flow velocity was similar. Hence, there was a significantly greater respiratory variation in superior vena cava systolic forward flow velocity in chronic obstructive pulmonary disease without an overlap with constrictive pericarditis (39.5+/-18.8 cm/s vs. 4.2+/-3.4 cm/s, p < 0.0001). CONCLUSIONS: Despite a similar respiratory variation in mitral E wave velocities, mitral inflow variables in chronic obstructive pulmonary disease are less restrictive compared with those in constrictive pericarditis. More importantly, patients with chronic obstructive pulmonary disease show a marked increase in inspiratory superior vena cava systolic forward flow velocity, which is not seen in patients with constrictive pericarditis.

Aged↗
PubMed1981

Peptide-induced prostaglandin biosynthesis in the renal-vein-constricted kidney.

The ipsilateral kidney was removed from a rabbit 48h after unilateral partial renal-vein-constriction and was perfused with Krebs-Henseleit media at 37 degrees C. Hourly administration of a fixed dose of bradykinin to the renal-vein-constricted kidney demonstrated a marked time-dependent increase in the release of bioassayable prostaglandin E(2) and thromboxane A(2) into the venous effluent as compared with the response of the contralateral control kidney. The renal-vein-constricted kidney produced up to 60 times more prostaglandin E(2) in response to bradykinin after 6h of perfusion as compared with the contralateral kidney; thromboxane A(2) was not demonstratable in the contralateral kidney. Inhibition of protein synthesis de novo in the perfused renal-vein-constricted kidney with cycloheximide lessened the hormone-stimulated increase in prostaglandin E(2) by 94% and in thromboxane A(2) by 90% at 6h of perfusion. Covalent acetylation of the renal cyclo-oxygenase by prior oral administration of aspirin to the rabbit inhibited initial bradykinin-stimulated prostaglandin E(2) biosynthesis 71% at 1h of perfusion. However, there was total recovery from aspirin in the renal-vein-constricted kidney by 2h of perfusion after bradykinin stimulation. Total cyclo-oxygenase activity as measured by [(14)C]arachidonate metabolism to labelled prostaglandins by renal cortical and renal medullary microsomal fractions prepared from 6h-perfused kidneys demonstrated that renal-vein-constricted kidney-cortical cyclo-oxygenase activity was significantly greater than the contralateral-kidney-cortical conversion, whereas medullary arachidonate metabolism was comparable in both the renal-vein-constricted kidney and contralateral kidney. These data suggest that perfusion of a renal-vein-constricted kidney initiates a time-dependent induction of synthesis of prostaglandin-producing enzymes, which appear to be primarily localized in the renal cortex. The presence of the synthetic capacity to generate very potent vasodilator and vasoconstrictor prostaglandins in the renal cortex suggests that these substances could mediate or modulate changes in renal vascular resistance in pathological states.

Animals↗
PubMed2004

Effusive-constrictive pericarditis.

BACKGROUND: Effusive-constrictive pericarditis is an uncommon pericardial syndrome characterized by concomitant tamponade, caused by tense pericardial effusion, and constriction, caused by the visceral pericardium. We conducted a prospective study of its clinical evolution and management. METHODS: From 1986 through 2001, all patients with effusive-constrictive pericarditis were prospectively evaluated. Combined pericardiocentesis and cardiac catheterization were performed in all patients, and pericardiectomy was performed in those with persistent constriction. Follow-up ranged from 1 month to 15 years (median, 7 years). RESULTS: A total of 1184 patients with pericarditis were evaluated, 218 of whom had tamponade. Of these 218, 190 underwent combined pericardiocentesis and catheterization. Fifteen of these patients had effusive-constrictive pericarditis and were included in the study. All patients presented with clinical tamponade; however, concomitant constriction was recognized in only seven patients. At catheterization, all patients had elevated intrapericardial pressure (median, 12 mm Hg; interquartile range, 7 to 18) and elevated right atrial and end-diastolic right and left ventricular pressures. After pericardiocentesis, the intrapericardial pressure decreased (median value, -5 mm Hg; interquartile range, -5 to 0), whereas right atrial and end-diastolic right and left ventricular pressures, although slightly reduced, remained elevated, with a dip-plateau morphology. The causes were diverse, and death was mainly related to the underlying disease. Pericardiectomy was required in seven patients, all of whom had involvement of the visceral pericardium. Three patients had spontaneous resolution. CONCLUSIONS: Effusive-constrictive pericarditis is an uncommon pericardial syndrome that may be missed in some patients who present with tamponade. Although evolution to persistent constriction is frequent, idiopathic cases may resolve spontaneously. In our opinion, extensive epicardiectomy is the procedure of choice in patients requiring surgery.

Adolescent↗
PubMed1975

Systolic time intervals in constrictive pericarditis. A study before and after digitalis.

Systolic time intervals were studied in 9 patients with documented constrictive pericarditis before and 15 to 20 minutes after intravenous administration of peruvoside (a quick acting digitalis-like glycoside) to determine underlying myocardial dysfunction. Data were compared with those of similarly studied normal subjects and patients with known myocardial dysfunction. Left ventricular ejection time index (LVETI) decreased in normal subjects (P less than 0.01) and in most patients with constrictive pericarditis, and increased marginally in those with myocardial dysfunction (NS) after peruvoside administration. Pre-ejection period index (PEPI) shortened significantly (P less than 0.01) after peruvoside in normal subjects and in patients with myocardial failure, but not in constrictive pericarditis. Likewise the predicted ejection fraction was insignificantly altered in constrictive pericarditis but significantly so (P less than 0.01) in myocardial failure and normal subjects. The response of one patient with constrictive pericarditis to parenteral peruvoside administration was similar to that seen in patients with myocardial failure. This patient had a delayed recovery after pericardiectomy. PEPI/LVETI ratio and ejection fraction were also abnormal in other patients with constrictive pericarditis when compared to normal subjects. Such abnormalities and the unusual response of some patients to administration of peruvoside may reflect underlying myocardial dysfunction in patients with constrictive pericarditis. However, it is possible that the rigid pericardium also contributes to these abnormalities to a varying extent. Systolic time indices and their response to digitalis appear to be a useful, atraumatic method for detecting underlying myocardial dysfunction in patients with constrictive pericarditis.

Adolescent↗
PubMed1987

Effect of age on the development of cardiac hypertrophy produced by aortic constriction in the rat.

To test the hypothesis that the capacity to develop left ventricular (LV) hypertrophy might diminish with advancing age, we examined the hypertrophic response to ascending aortic constriction in 3 groups of adult Fischer 344 rats (9 months, 18 months, and 22 months of age). Aortic constriction was created so that aortic cross-sectional areas would be the same for the 3 groups of rats. Four weeks after imposition of aortic constriction, there was no significant difference in peak LV pressure, peak-to-peak and mean systolic pressure gradients between left ventricle and aorta, cardiac output, LV minute work, or cross-sectional area of the aortic constrictions in the 3 groups. In 9-month-old aortic-constricted rats, LV dry wt (LVDW)/body wt, LVDW/tibial length, and myocyte width increased by 23% (p less than 0.01), 14% (p less than 0.01), and 27% (p less than 0.01), respectively, compared with sham-operated rats. In contrast, in 18-month-old and 22-month-old aortic-constricted rats, LVDW/body wt and LVDW/tibial length were unchanged compared with sham-operated controls, and increases in myocyte width were only modest 4 weeks following constriction. RNA concentration in the myocardium 5 days after constriction increased by 21% (p less than 0.001) in 9-month-old rats but showed no significant rise in 18-month-old rats. These results suggest that advancing age is associated with a diminished capacity to develop myocardial hypertrophy in response to acute pressure overload and that a reduced ability to synthesize protein may be one of the major contributing factors to a diminished capacity for hypertrophy in advanced age.

Aging↗
PubMed1977

Cyclical reduction in blood flow of partially constricted coronary artery in dogs. II. An arteriographic study.

Mechanisms for cyclical reduction in peripheral blood pressure and flow of partially constricted coronary artery of anesthetized dogs has been examined. In 64 of 97 preparations, cyclical reduction in coronary blood pressure and flow developed 3 to 32 min after the beginning of constriction. Period duration of the cyclical reduction ranged from 1 to 32 min. The cyclical reduction was frequently associated with elevation of the ST segment of surface electrocardiogram, systolic bulge of the left ventricle and excitation of afferent cardiac sympathetic nerve fibers. In the preparations in which cyclical reduction was not produced by constriction, a brief stretching of the constricted portion provoked the cyclical reduction. Segmental or diffuse narrowing of the constricted coronary artery which occurred during the reduction in pressure and flow was demonstrated by selective arteriography. Also, segmental spasm in the constricted coronary artery was demonstrated by photography. No obvious difference in the constricted of the artery was observed histologically between the preparations in which cyclical reduction developed and those in which cyclical reduction was not produced. The results indicate participation of vasospasm in the cyclical reduction of blood pressure and flow in partially constricted coronary artery.

Action Potentials↗
PubMed2005

A new protocol for maxillary protraction in cleft patients: repetitive weekly protocol of alternate rapid maxillary expansions and constrictions.

OBJECTIVE: It was hypothesized that, through a repetitive weekly protocol of Alternate Rapid Maxillary Expansions and Constrictions (Alt-RAMEC), the maxilla in cleft patients could be protracted more effectively than with a single course of rapid maxillary expansion (RME). METHODS: Twenty-six consecutive unilateral cleft lip and palate patients at the age of mixed dentition were included in this prospective clinical study. The rapid maxillary expansion group included the first 16 consecutive patients undergoing 1 week of rapid maxillary expansion (1 mm/day) followed by 5 months, 3 weeks of maxillary protraction. The Alternate Rapid Maxillary Expansions and Constrictions group included the next 10 consecutive patients undergoing 9 weeks of Alternate Rapid Maxillary Expansions and Constrictions followed by 3 months, 3 weeks of maxillary protraction. Daily activation of the weekly expansion or constriction was 1.0 mm. Two-hinged expanders and intraoral maxillary protraction springs were used in both groups. Treatment results were evaluated cephalometrically. RESULTS: The amount of maxillary anterior displacement by the 2-hinged expander in the Alternate Rapid Maxillary Expansions and Constrictions group was 3.0 +/- 0.9 mm at A point, significantly greater than the 1.6 +/- 1.0 mm in the rapid maxillary expansion group. The amount of maxillary advancement with intraoral protraction springs in the Alternate Rapid Maxillary Expansions and Constrictions group was 2.9 +/- 1.9 mm at A point, significantly greater than the 0.9 +/- 1.1 mm in the rapid maxillary expansion group. The overall amount of maxillary advancement in the Alternate Rapid Maxillary Expansions and Constrictions group was 5.8 +/- 2.3 mm at A point. This result remained stable, without significant relapse after 2 years. CONCLUSIONS: Maxillary protraction using the 2-hinged expander, a repetitive weekly protocol of Alternate Rapid Maxillary Expansions and Constrictions, and intraoral protraction springs is most effective, with stable results at 2-year follow-up.

Cephalometry↗
PubMed1995

Luminal constrictions due to endothelial cells in capillaries of mouse exocrine pancreas.

During our recent studies of the capillaries in exocrine pancreas of mouse, numerous local constrictions which reduced the luminal diameter were observed both by scanning electron microscopy of corrosion casts and by in vivo microscopy. In the present study we have identified the features responsible for the constrictions and compared the diameters of vessels and constrictions measured using the two methods. A simple theoretical model was used to predict the effects of such constrictions on blood flow in the acinar capillaries of the pancreas. Intravital observations revealed that bulging endothelial cells were primarily responsible for the constrictions. For samples of 100 measurements, good agreement was found between the mean capillary diameters from casts (6.3 microns +/- 0.50 SD) and in vivo (6.2 microns +/- 0.53 SD), but the mean diameter measurement at constrictions was greater (P < 0.01) in casts (3.9 microns +/- 0.84 SD) than in vivo (3.5 microns +/- 1.05 SD). Topical application of norepinephrine caused endothelial nuclear regions to bulge into the capillary lumen, decreasing the mean diameter at these locations to 3.3 microns +/- 0.9 (SD, n = 21). Based on the 100 in vivo measurements, the theoretical model predicted that, on average, the constrictions would reduce flows to 51% of those in fully open vessels. It is unlikely, however, that the constrictions observed in acinar capillaries of the pancreas of mouse would result in significant blockage of the vessels by red blood cells.

Animals↗
PubMed1992

An experimental painful peripheral neuropathy due to nerve constriction. I. Axonal pathology in the sciatic nerve.

A constriction injury to the sciatic nerve of the rat produces a painful peripheral neuropathy that is similar to the conditions seen in man. The pathology of the sciatic nerve in these animals was examined at 10 days postinjury, when the abnormal pain sensations are near maximal severity. The nerves were examined with (1) complete series of silver-stained longitudinal sections of pieces of the nerve (3 cm or more) that contained the constriction injury in the center, (2) toluidine blue-stained semithin sections taken at least 1 cm proximal and 1 cm distal to the constriction, and (3) EM sections taken adjacent to those stained with toluidine blue. One centimeter or more proximal to the constriction, both myelinated and unmyelinated axons were all normal. Nearer to the constriction, extensive degeneration of myelinated axons became increasingly common, as did signs of endoneurial edema. Distal to the constriction, the nerve was uniformly edematous and full of myelinic degeneration. There was a profound loss of large myelinated axons and a distinctly less severe loss of small myelinated and unmyelinated axons. These observations show that at 10 days postinjury the constriction produces a partial and differential deafferentation of the sciatic nerve's territory. The absence of degeneration in the nerve 1 cm proximal to the constriction indicates the survival of the primary afferent neurons whose axons are interrupted.

Animals↗
PubMed1994

Selective constriction of small cutaneous arteries by NPY matches distribution of NPY in sympathetic axons.

This study has begun to investigate some functional implications of the differential localization of neuropeptide Y (NPY) in sympathetic neurons supplying different arterial segments in the cutaneous circulation of the guinea-pig ear. Responses of the main ear artery to exogenous NPY and norepinephrine (NE) were examined in vitro by measuring isometric tension. Responses of smaller arterial vessels to application of exogenous NPY or NE to the adventitial surface were examined in anaesthetized, ventilated guinea-pigs, by measuring changes in internal vessel diameter using video microscopy. Some arterial segments subsequently were examined for the presence of immunoreactivity (IR) to tyrosine hydroxylase (TH) and NPY. NPY (1 nM-10 microM) contracted the main ear artery (EC50 = 10 nM; max. contraction = 30% KCl), and 1 nM NPY produced slight potentiation of contractions produced by NE. In vivo, local applications of NPY (1-10 microM) constricted only a subpopulation of arterial vessels (23 of 41). All vessels constricted by NPY were innervated by axons containing IR to both TH and NPY, and as a population, were more proximal in the arterial tree (branch orders 3 to 6) than were vessels insensitive to NPY (branch orders 4 to 8). Most vessels insensitive to NPY were arterioles and arterio-venous anastomoses < 40 microns in diameter, which were innervated by axons containing TH-IR but not NPY-IR. In contrast, local application of NE (1-30 microM) constricted all vessels examined in vivo. When present, NPY constrictions had a longer latency (15-45 s) and duration (3-4 min) than NE constrictions of the same vessel segments. In vivo, NPY sometimes potentiated the peak amplitude of NE constrictions (2 of 7 vessels), but only in vessels where NPY also produced direct constriction. These results reveal an excellent correlation between the localization of NPY in sympathetic axons, and the location of postsynaptic NPY receptors throughout the cutaneous arterial system. Any NPY released in response to strong activation of cutaneous sympathetic neurons is likely to act preferentially on the proximal cutaneous arteries, and to lead to a more prolonged constriction of these arteries than of more distal arterioles and arterio-venous anastomoses.

Adrenergic Fibers↗
PubMed1996

Origin of beading constrictions at the axolemma: presence in unmyelinated axons and after beta,beta'-iminodipropionitrile degradation of the cytoskeleton.

Myelinated nerve fibres become beaded when nerves are subjected to a mild stretch; the beading is seen as varicosities, a series of alternating constrictions and enlargements, when using freeze-substitution or cold-fixation to hold this labile form change in place during fixation. One possibility for how this form change comes about is that the myelin sheath or its Schwann cell initiates beading. We now report, however, that a similar beading is seen in the axons of unmyelinated fibres. In electron micrographs, longitudinal sections of axons show the series of constrictions and expansions typical of beading. In cross-sections, axons with unusually small diameter, corresponding to the constrictions, are seen to contain closely packed microtubules and neurofilaments while neighbouring swollen axons with widely dispersed microtubules correspond to the beading expansions. Another possibility for the form change is that the cytoskeleton is responsible for beading. We discovered that direct exposure of nerves to beta, beta'-iminodipropionitrile in vitro for 1-6 h causes both axonal microtubules and neurofilaments to become degraded and replaced by an amorphous residue. Nevertheless, beta,beta'-iminodipropionitrile-treated nerves show constrictions in myelinated fibres when stretched. An even greater degree of beading with narrower and longer constrictions appears in some fibres, with the expanded regions having oblate ends giving the appearance of a string of sausages. In cross-sections taken through the constrictions, a greater than usual reduction of axonal area was seen, this was due to the loss of cytoskeletal organelles which would act to limit the degree of constriction. With longer exposure to beta, beta'-iminodipropinitrile more fibres show complete degeneration of the cytoskeleton and form ovoids typical of Wallerian degeneration. Unmyelinated axons of beta, beta'-iminodipropionitrile-treated nerves which showed degeneration of their cytoskeleton with its replacement by amorphous material still demonstrated beading. As neither the myelin sheath nor the intact cytoskeleton within the axon is necessary for beading, by exclusion, we consider beading constrictions to be initiated at the level of the axolemma. In our hypothesis the membrane skeleton is responsible; namely, the spectrin, actin and other molecular species lining the inside of the axolemma and binding to transmembrane proteins. The membrane skeleton may be activated by stretch via transmembrane proteins (e.g. beta 1-integrins). The membrane skeleton mechanism may also be directly engaged in the production of Wallerian degeneration or be induced by neurotoxic agents.

Animals↗